We have selected environmental tobacco smoke (ETS) as a "model" carcinogenic exposure which also represents a major public health concern. It is estimated that in the U.S. 30% of adults are smokers and 42% of children are regularly exposed to ETS. Conventional epidemiologic studies of the cancer risk of passive smoking have been severely limited by inadequate exposure data. Moreover, there is evidence that children may have heightened susceptibility to environmental carcinogens such as ETS. Therefore, we propose a cross-sectional study of preschool children and their biologic mothers who will be recruited from a Dominican population in New York City. The central hypotheses to be tested are: (1) Young children have higher levels of biomarkers than related adults when environmental exposure is comparable, indicating their greater susceptibility to carcinogens due to developmental factors. (2) Children's levels of biomarkers are correlated with those of their mothers, suggesting a genetic component in biologic response. This study will use several complementary biologic markers as proxies for the carcinogenic fraction of ETS. In addition to cotinine, samples will be assayed for protein adducts formed by the carcinogens 4-aminobiphenyl and polycyclic aromatic hydrocarbons, SCEs and oncogene protein products of the ras, myc, and fes genes. While the major focus is on the relationship between passive smoking and biologic markers, our study design also allows us to evaluate the "dose-response" for smoking in women of the same age, ethnic background, socioeconomic status and geographic local. This research will build upon our prior "range-finding" studies in adults and is a prerequisite to large-scale "molecular epidemiologic" studies. The outcome of this study may have significant implications for risk assessment theory and practice.